Plus Lens Therapy for Myopia Prevention (was Sci Proof that the eye is dynamic)

Discussion in 'Eye-Care' started by Dr Judy, Aug 11, 2004.

  1. Dr Judy

    Dr Judy Guest

    The other thread was getting too long and onto a new topic. Here is a
    summary of some of the research that advocates of using a plus lens refer to
    and my usual questions. For ease of reading I will post the study title and
    comments, the full abstracts follow.

    Basic description of the emmetropization process:
    Optom Vis Sci. 1998 Jun;75(6):388-98. Related Articles, Links

    Spectacle lenses and emmetropization: the role of optical defocus in
    regulating ocular development.
    Smith EL 3rd.

    Smith states that young monkey eyes rapidly change to effective emmetropia
    for the effective refractive error simulated by + or - lenses. When the
    simulating lenses are removed, leaving the eyes either myopic or hyperopic,
    the eyes rapidly change to emmetropia. The process is independant of
    accommodation.

    J Comp Physiol [A]. 1996 Aug;179(2):185-94. Related Articles, Links

    Chick eye optics: zero to fourteen days.
    Irving EL, Sivak JG, Curry TA, Callender MG.
    Department of Ophthalmology, University of Toronto, Ontario, Canada.

    Authors describe development of normal chicken eyes. Chicks are born with
    hyperopia and become emmetropic by age 14 days.

    Vis Neurosci. 1990 Feb;4(2):177-83. Related Articles, Links

    Developing eyes that lack accommodation grow to compensate for imposed
    defocus.
    Schaeffel F, Troilo D, Wallman J, Howland HC.
    Section of Neurobiology and Behavior, Cornell University, Ithaca, New York.

    The emmetropization mechanism in neonatal chicks is not linked to
    accommodation.

    So we see that young animal eyes somehow recognize that refractive error is
    present and growth is regulated so that emmetropia is achieved. I would
    suggest that if refractive error is present in individual human school age
    children or adults then those individuals have not inherited a fully
    functional emmetropization mechanism, their mechanism does not respond in
    the usual way to refractive defocus. The use of plus to change their
    refractive error is unlikely to work because those individuals do not
    respond to defocus; effectively the very existence of myopic refractive
    error means that the eye is unusual and plus lenses will not work.

    Further, as accommodation is not a factor in this process, near work is
    unlikely to be a cause of myopia

    Some studies with relevance to "stair case myopia" -- the idea that
    correcting myopia will induce progression of myopia.

    Vision Res. 2000;40(23):3273-82. Related Articles, Links


    Optical correction of form deprivation myopia inhibits refractive recovery
    in chick eyes with intact or sectioned optic nerves.
    Wildsoet CF, Schmid KL.
    School of Optometry, University of California, 94720-2020, Berkeley, CA,
    USA.

    Chicks eyes with experimentally induced myopia will change back to
    emmetropia when the myopia inducing treatment was removed. In this
    experiment, experimentally induced myopia was fully corrected or
    undercorrected with minus lenses. Chick eyes stabilized their myopia at a
    level consistent with the correcting lens power used, myopia did not
    progress with use of correcting lens.

    Vision Res. 1991;31(4):717-34
    Properties of the feedback loops controlling eye growth and refractive state
    in the chicken.
    Schaeffel F, Howland HC.
    Forschungsstelle fur Experimentelle Ophthalmologie, Tubingen, F.R.G.

    In this experiment, chicks with experimentally induced myopia and hyperopia
    were provided with correcting minus or plus lenses. Some, but not all, eyes
    become emmetropic despite the use of the lenses, ie chicks wearing minus
    became less myopic!


    Finally, a recent study that simulates the conditions that some claim causes
    myopia in Asian children: spending lots of time reading. The reading was
    simulated with high minus lenses, similar to reading at 6 inches all day.
    Chicks given 8 minutes a day of plus lens wear (simulaing a high myope
    wearing no glasses) or given 8 minutes a day of no lens wear (simulating
    distance viewing by a myope wearing glasses or an emmetrope) did not
    develop myopia. This suggests to me that a plus lens is not needed to
    prevent myopia development in eye with a functional emmetropization
    mechanism; a few minutes a day of distance viewing is all that is needed.

    Invest Ophthalmol Vis Sci. 2003 Jul;44(7):2818-27. Related Articles,
    Links


    Potency of myopic defocus in spectacle lens compensation.
    Zhu X, Winawer JA, Wallman J.
    Department of Biology, City College of the City University of New York, New
    York, New York 10031, USA

    My conclusion to a review of the literature is that an inherited functional
    emmetropization mechanism is needed to prevent myopia development. If an
    eye has this mechanism, it will not develop myopia and the use of plus
    lenses is not needed and may cause hyperopia. If an eye does not have this
    mechanism, then it will not respond in the usual predictable way to plus
    lenses and will likely develop myopia anyway.

    Dr Judy

    Ophthalmic Physiol Opt. 1992 Oct;12(4):448-56.
    Refractive plasticity of the developing chick eye.

    Irving EL, Sivak JG, Callender MG.

    School of Optometry, University of Waterloo, Ontario, Canada.

    We have developed a lightweight plastic goggle with rigid contact lens
    inserts that can be applied to the eyes of newly hatched chicks to explore
    the range and accuracy of the developmental mechanism that responds to
    retinal defocus. Convex and concave lenses of 5, 10, 15, 20 and +30 D were
    applied to one eye on the day of hatching. The chick eye responds accurately
    to defocus between -10 and +15 D, although hyperopia develops more rapidly
    than myopia. Beyond this range there is first a levelling off of the
    response and then a decrease. The resulting refractive errors are caused
    mainly by increases and decreases in axial length, although high levels of
    hyperopia are associated with corneal flattening. If +/- 10 D defocusing
    lenses are applied nine days after hatching the resulting myopia and
    hyperopia are equal to about 80% of the inducing power. After one week of
    inducing myopia and hyperopia with +/- 10 D lenses, the inducing lenses were
    reversed. In this case, the refractive error did not reach the power of the
    second lens after another week of wear. Instead, astigmatism in varying
    amounts (0-12 D) was produced, being greater when reversal was from plus to
    minus. Finally, astigmatism can also be produced by applying 9 D toric
    inducing lenses on the day of hatching. The astigmatism produced varies from
    2 to 6 D, and the most myopic meridian coincides with the power meridian of
    the inducing lens. This astigmatism appears to be primarily due to corneal
    toricity.(ABSTRACT TRUNCATED AT 250 WORDS)


    Optom Vis Sci. 1991 May;68(5):364-8.
    Inducing myopia, hyperopia, and astigmatism in chicks.

    Irving EL, Callender MG, Sivak JG.

    School of Optometry, University of Waterloo, Ontario, Canada.

    Myopia and hyperopia have been produced in chicks by applying specially
    designed convex and concave soft contact lenses to the eyes of newly hatched
    birds. After 2 weeks of wear, the eyes develop refractive states equivalent
    in sign and amount (+8 and -10 D) to the lens used. However, the lenses
    produce an artificial hyperopic shift during the first week of wear due to
    corneal flattening. We have developed a new approach involving the use of
    goggles with hard convex and concave contact lens inserts placed between the
    frontal and lateral visual fields. Myopia and hyperopia (+10 and -10 D) can
    be produced within days (4 days for hyperopia and 7 days for myopia) if the
    defocus is applied from the day of hatching. We can also produce significant
    amounts of astigmatism (1 to 5 D) axis at 90 degrees and 180 degrees by
    using cylindrical contact lens inserts. Although these last results are
    preliminary, they suggest that accommodation is not likely involved at this
    stage of refractive development because we do not believe that the
    accommodative mechanism can cope with cylindrical defocus. All spherical
    refractive errors produced using the goggle system appear to result from
    alterations in vitreous chamber depth.
    Ciba Found Symp. 1990;155:160-72; discussion 172-7. Related Articles,
    Links



    Vis Neurosci. 1990 Feb;4(2):177-83. Related Articles, Links


    Developing eyes that lack accommodation grow to compensate for imposed
    defocus.

    Schaeffel F, Troilo D, Wallman J, Howland HC.

    Section of Neurobiology and Behavior, Cornell University, Ithaca, New York.

    The eyes of growing chicks adjust to correct for myopia (eye relatively long
    for the focal length of its optics) or hyperopia (eye relatively short for
    the focal length of its optics). Eyes made functionally hyperopic with
    negative spectacle lenses become myopic and long, whereas eyes made
    functionally myopic with positive spectacle lenses become hyperopic and
    short. We report here that these compensatory growth adjustments occur not
    only in normal eyes but also in eyes unable to accommodate (focus) because
    of lesions to the Edinger-Westphal nuclei. Thus, at least in chicks,
    accommodation is not necessary for growth that reduces refractive errors
    during development, and may not be necessary for the normal control of eye
    growth.


    Optom Vis Sci. 1998 Jun;75(6):388-98. Related Articles, Links


    Spectacle lenses and emmetropization: the role of optical defocus in
    regulating ocular development.

    Smith EL 3rd.

    College of Optometry, University of Houston, Texas, USA.

    The purpose of our investigation was to determine whether early ocular
    growth and refractive development was regulated by visual feedback in infant
    monkeys. Specifically, we examined the ability of infant monkeys to
    compensate for optically induced changes in the eye's refractive state and
    to recover from experimentally induced refractive errors. For
    moderate-powered anisometropic lenses, infants exhibited differential
    interocular axial growth rates that reduced the lens-induced refractive
    imbalance between the two eyes. Infants treated with equal-powered lenses
    over both eyes also showed compensating growth. For lens powers between
    approximately -3 and +6 D, the resulting refractive-error changes, which
    were primarily due to alterations in vitreous chamber growth rates, were
    well correlated with the effective refractive state produced by the
    treatment lenses. When the stimulus for altered eye growth was removed and
    the infants were provided unrestricted vision, monkey eyes consistently grew
    toward emmetropia. The remarkable degree of adaptability exhibited by the
    eyes of infant monkeys demonstrates that emmetropization in this higher
    primate is an active process that is regulated on a continuous basis by
    optical defocus. Consequently, early in life spectacle lenses by changing
    the eye's effective focus can predictably alter ocular growth and the
    refractive status of one or both eyes.

    Vision Res. 2000;40(23):3273-82. Related Articles, Links


    Optical correction of form deprivation myopia inhibits refractive recovery
    in chick eyes with intact or sectioned optic nerves.

    Wildsoet CF, Schmid KL.

    School of Optometry, University of California, 94720-2020, Berkeley, CA,
    USA.

    The finding that the eyes of young chicks recover quickly from form
    deprivation myopia (FDM) has been interpreted as indirect evidence for
    active emmetropization. More direct evidence would be the demonstration that
    correction of FDM with spectacle lenses, thereby removing the defocus
    signal, prevents recovery. We investigated this issue in eyes with intact
    and sectioned (ONS) optic nerves. Previous studies suggest that an intact
    optic nerve is necessary for accurate emmetropization. Seventy day-old male
    chicks were monocularly deprived using velcro-mounted diffusers, which were
    removed after 5-6 days and in some (n=51), but not all cases, replaced by
    spectacle lenses (-5, -10 or -15 D). Approximately half (n=34) of the chicks
    also underwent ONS on day 1. Refractive errors and axial ocular dimensions
    were measured when the diffusers were first removed and thereafter at 2-4
    day intervals over the following 1-2 weeks. In one case, measurements were
    continued at less regular intervals to 33 days. Lens powers were selected to
    either approximately correct or under-correct the refractive errors present
    when the diffusers were removed. Form deprivation in normal chicks produced
    large myopic shifts in refraction (means for groups range from -9.20
    to -16.07 D). When the deprivation treatment was terminated, the myopia
    quickly decreased to negligible levels unless optically corrected.
    Correcting lenses stabilized the myopia to a level consistent with the lens
    power used. Interocular differences in axial length were consistent with an
    axial origin to the refractive changes. Results for the ONS groups exhibited
    similar trends although there was increased variability in the data. The
    findings support the interpretation that recovery from FDM is a product of
    active emmetropization. That ONS increased the variability of such responses
    implies that an intact optic nerve is required for accurate emmetropization.

    Related Articles, Links


    J Comp Physiol [A]. 1996 Aug;179(2):185-94. Related Articles, Links


    Chick eye optics: zero to fourteen days.

    Irving EL, Sivak JG, Curry TA, Callender MG.

    Department of Ophthalmology, University of Toronto, Ontario, Canada.

    Ocular dimensions and refractive state data for chicks 0 to 14 days of age
    were obtained from 234 untreated control eyes of birds treated unilaterally
    in previous work involving various defocussing lenses and/or translucent
    goggles. Refractive state and corneal curvatures were measured in vivo by
    retinoscopy and ophthalmometry respectively. Intraocular dimensions were
    measured by A-scan ultrasonography, after which the eyes were removed,
    weighed and measured. In some cases (n = 52) intraocular dimensions and lens
    curvatures were obtained from frozen sections of enucleated eyes. The
    hyperopia of hatchling chicks (+6.5 +/- 4.0 D) initially decreases rapidly
    and then more gradually to +2.0 +/- 0.5 D by 16 days. The distribution of
    refractive errors is very broad at Day 0, but becomes leptokurtotic, with a
    slight myopic skew, by Day 14. Corneal radius is constant for the first four
    days, possible as a result of pre-hatching lid pressure, and then increases
    linearly, as do all lens dimensions, axial diameter and equatorial diameter.
    Schematic eyes were developed for Days 0, 7, and 14.

    Vision Res. 1996 Apr;36(7):1023-36. Related Articles, Links


    Effects on the compensatory responses to positive and negative lenses of
    intermittent lens wear and ciliary nerve section in chicks.

    Schmid KL, Wildsoet CF.

    Centre for Eye Research, Queensland University of Technology and Vision,
    Brisbane, Australia.

    This study examined the ocular compensation to lens-induced defocus in chick
    and the effect of interrupting lens wear on a daily basis. Eyes fitted with
    +10 D lenses at hatching compensated rapidly, with almost complete
    compensation after 4 days of lens wear; they had decreased vitreous chamber
    depth compared to normal eyes and were thus hyperopic when the lenses were
    removed. In contrast, adaptation to the -10 D lenses was much slower, was
    still incomplete after 9 days of lens wear, and in this case, eyes had
    increased vitreous chamber depth and were myopic without the lenses.
    Adaptation improved when lens wear was delayed until 7 days after hatching.
    The effect of interrupting lens wear by periods of normal vision varied with
    the sign of the lenses worn. Hyperopia was always seen in response to +10 D
    lenses, although the magnitude of the response decreased as the duration of
    lens wear was decreased. In contrast, even brief periods of normal vision,
    i.e., 3 hr, prevented the development of myopia in response to the -10 D
    lenses; this apparent sensitivity to normal vision is similar to that
    reported for form-deprivation myopia. Ciliary nerve section used here to
    eliminate accommodation did not alter these response patterns.


    Vision Res. 1991;31(4):717-34
    Properties of the feedback loops controlling eye growth and refractive state
    in the chicken.

    Schaeffel F, Howland HC.

    Forschungsstelle fur Experimentelle Ophthalmologie, Tubingen, F.R.G.

    Recent experiments in chickens provide evidence that axial eye growth and
    refractive state are guided by mechanisms sensitive to refractive error. To
    determine whether or not the sign of refractive error is derived from
    longitudinal chromatic aberration we raised chicks with spectacle lenses in
    monochromatic light. The eyes showed an appropriate growth response to
    correct for the defocus imposed by the lenses no different than in previous
    experiments in white light. Thus, in normally accommodating chicks chromatic
    cues are not necessary for emmetropization to occur. We examined the
    linearity of feedback loops controlling axial eye growth: positive spectacle
    lenses were found to inhibit axial growth very efficiently making the eyes
    shorter than normal whereas negative lenses had little effect on axial
    elongation: feedback loops for regulation of axial growth are highly
    nonlinear and act most efficiently on the myopic side. We found that,
    subsequent to a period of binocular deprivation of form vision, the
    refractive errors acquired are highly correlated in both eyes. Since both
    eyes grew without visual feedback we conclude that the gains in the feedback
    loops that control axial growth must be similar in both eyes. We suggest
    that the gains are genetically determined and are typical for each
    individual. Chicks made near-sighted in both eyes by "deprivation of form
    vision" were corrected by appropriate negative lenses. Three out of five
    chicks recovered from myopia despite the correction. Also two chicks that
    were made near-sighted in one eye recovered with no regard to the correcting
    lens. Three chicks remained more myopic than the correcting lens required
    and finally started to recover while the lens was still in place. Two out of
    three chicks that were made far-sighted showed recovery despite appropriate
    correction by positive lenses. We conclude that there must be a nonvisual
    mechanism highly sensitive to abnormal eye shape. During expt (4) we found
    unexpectedly that the development of form deprivation myopia is inhibited if
    no part of the retina in an animal is exposed to normal visual experience.
    The result indicates that some communication between both eyes exists,
    although form deprivation myopia itself has been shown to develop
    independently in both eyes.



    Invest Ophthalmol Vis Sci. 2003 Jul;44(7):2818-27. Related Articles,
    Links


    Potency of myopic defocus in spectacle lens compensation.

    Zhu X, Winawer JA, Wallman J.

    Department of Biology, City College of the City University of New York, New
    York, New York 10031, USA.

    PURPOSE: Previous studies have shown that chick eyes compensate for positive
    or negative lenses worn for brief periods if the chicks are in darkness the
    remainder of the time. This study was undertaken to determine whether chicks
    can compensate for brief periods of lens wear if given unrestricted vision
    the remainder of the time. Previous studies have also shown that chick eyes
    alternately wearing positive and negative lenses for brief periods
    compensate for the positive lenses. The current study sought to determine
    whether brief periods of positive lens wear can outweigh daylong wearing of
    negative lenses. METHODS: Chicks wore +6 D or +10 D lenses for between 8 and
    60 min/d, in two to six periods and wore either no lenses or negative lenses
    for the remainder of the 12-hour daylight period. Refraction and ultrasound
    biometry were performed before and after the 3-day-long experiments.
    RESULTS: Wearing positive lenses for as little as 12 min/d (six periods of 2
    minutes) with unrestricted vision the remainder of the time caused eyes to
    become hyperopic and reduced the rate of ocular elongation. These effects
    also occurred when the scene viewed was beyond the far point of the
    lens-wearing eye and thus was myopically blurred. Even when chicks wore
    negative lenses for the entire day except for 8 minutes of wearing positive
    lenses, the eyes compensated for the positive lenses, as though the negative
    lenses had not been worn. When chicks wore binocular negative lenses for the
    entire day except for 8 minutes of wearing a positive lens on one eye and a
    plano lens on the other, the eye wearing the positive lens became less
    myopic than the eye wearing the plano lens. CONCLUSIONS: Brief periods of
    myopic defocus imposed by positive lenses prevent myopia caused by daylong
    wearing of negative lenses. This implies that periods of myopic and
    hyperopic defocus do not add linearly. If children are like chicks and if
    the hyperopic defocus of long daily periods of reading predisposes a child
    to myopia, regular, brief interruptions of reading might have use as a
    prophylaxis against progression of myopia.
     
    Dr Judy, Aug 11, 2004
    #1
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  2. Dr Judy

    Cathy Hopson Guest

    We are agreed (finally) as to accommodation. Your previous help with
    explanations of accommodation has been excellent, not to mention the studies
    that have been offered that eliminate accommodation as the cause. Hyperopic
    defocus, however, where the stimulus is too near to see focused if not
    accommodated for, is another matter. Young animal retinas recognize the
    defocus (probably before accommodating for it) and grow to correct the
    refractive error. In human school age children and adults, the same
    hyperopic defocus is recognized by the retina and is corrected via the same
    process of emmetropization. The inducement is the near work they do. In
    animals, it is the minus lenses. Where do you see myopes not responding in
    the usual way to refractive defocus? The mechanism is there and is fully
    functional. The ones not responding to near work defocus are emmetropes and
    hyperopes. Why are their retinas not responding in the same way as myopes
    and animals? The defocus is obviously there.

    I'm hearing a Dr Judy question pop up. Why do hyperopes exist? I ask back,
    is it really because their emmetropization mechanism is fully functional, or
    is it because the mechanism is circumvented or not yet triggered? From the
    studies, placing high minus lenses on them all day will induce myopia.

    Cathy
     
    Cathy Hopson, Aug 12, 2004
    #2
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  3. Dr Judy

    Cathy Hopson Guest

    If only we could remove the myopia inducing factors in humans, we'd be set.
    Since we don't, doesn't the correcting lens power merely serve to reset the
    0.0 point? That's the primary blame placed on the minus lenses by the near
    work crowd. The peripheral defocus crowd have to take a different tack.
    Either way, it's the continuing myopia inducing factors that require an
    alternate intervention.

    Cathy
     
    Cathy Hopson, Aug 12, 2004
    #3
  4. Dr Judy

    Cathy Hopson Guest

    Aha! A risk is exposed. Astigmatism was produced in greater amounts when
    reversal was from one week of full time plus to one week of full time minus
    than from minus to plus. Our discussion is not advocating pulling someone
    to extreme hyperopia then to extreme myopia, so the risk of brief periods of
    plus each day to maintain existing myopia is negligible.

    Cathy
     
    Cathy Hopson, Aug 12, 2004
    #4
  5. Dr Judy

    Cathy Hopson Guest

    This abstract introduces the idea that the eyes communicate with each other
    to overrule different inducements given each eye independently. At least,
    that's what their conclusion was getting at. This shouldn't prove
    unpredictability under normal circumstances and it hasn't stopped minus
    prescriptions for myopia, so it shouldn't stop plus prescriptions for
    stopping progression. With more data, don't you think they'd find a
    predictable pattern? It does show plus works faster than minus as an
    inducement, like the other studies.

    Cathy
     
    Cathy Hopson, Aug 12, 2004
    #5
  6. Dr Judy

    Cathy Hopson Guest

    Your facts are incorrect. Please reread the abstract.

    8 mins. of plus maintained emmetropia after wearing minus lenses all day.
    These chicks could never focus all day long (unless accommodation was strong
    enough). They had hyperopic defocus (in spite of accommodation) all day
    except for the 8 mins. of myopic defocus.

    8 mins. of plus produced hyperopia after wearing no lenses all day (not 8
    mins. of no lenses after all day of minus). These chicks could focus all
    day except for the 8 mins. in plus. The plus time does not simulate
    distance viewing by a myope wearing glasses or an emmetrope. It is 8 mins.
    of myopic defocus, just like above.

    Your conclusion that a plus lens is not needed to counter all day minus, and
    that plus is unpredictable, will have to be revised to account for the
    correct facts.

    The 1996 abstract by Schmid/Wildsoet showed "brief periods" unrestricted was
    successful in countering the -10D inducement. I don't think anyone would
    consider 3 hours/day to be brief, so this scheme is unusable as treatment,
    even for the quick-changing eye shape of chicks.

    I hope to read a revised conclusion to a review of the literature as well.
    There is no example of myopia developing using a plus lens strong enough and
    long enough to counter myopia inducing behaviors and stimuli. There is also
    no example in the literature of the emmetropization mechanism not
    functioning predictably under normal circumstances.

    Cathy
     
    Cathy Hopson, Aug 12, 2004
    #6
  7. Dr Judy

    Cathy Hopson Guest

    Vision Res. 1995 May;35(9):1211-6. Related Articles, Links


    Differences in eye growth and the response to visual deprivation in
    different strains of chicken.

    Troilo D, Li T, Glasser A, Howland HC.

    New England College of Optometry, Boston, MA 02115, USA.

    Several laboratories studying visual deprivation myopia in the domestic
    chick report varying degrees of axial elongation and myopia induced by
    similar visual deprivation techniques. In this study we tested the
    hypothesis that in different strains of chick the eyes respond differently
    to visual deprivation. We compared under identical conditions two strains of
    White Leghorn chick commonly used in ocular development research--the
    Cornell-K strain (K) and Washington H & N Strain (H/N). The normal
    development of the eye was found to vary significantly between these strains
    of White Leghorn chicks. The K strain normally develops flatter corneas,
    thicker lenses, and larger eyes than the H/N strain. The response to visual
    deprivation also varies significantly between strains. For example, we find
    that 2 weeks of visual deprivation in the K strain results in less
    elongation of the vitreous chamber and flattening of the cornea yielding
    lower levels of induced myopia compared to the H/N strain. Our results show
    that while visual experience clearly affects normal ocular development in
    both strains of chick, the nature of the effect depends upon not only the
    type and duration of the experience but the genetics of the subject
    population as well.

    PMID: 7610582 [PubMed - indexed for MEDLINE]



    Is this the basis of the genetic argument? Are myopes, emmetropes, and
    hyperopes professed to be from different strains of humans? Are 20% of
    twins supposed to be from different strains, also? I looked up other
    abstracts by HC
    Howland to see what he might be talking about in his 1991 feedback loop
    abstract. He and Schaeffel are still studying it this way in strains of
    mice in 2004.

    Cathy
     
    Cathy Hopson, Aug 12, 2004
    #7
  8. Dr Judy

    Dr Judy Guest

    Rather than respond to each of your posts, here is an overview reply

    My purpose in the original post was to provide a taste of the research and
    add my comments. A search on PubMed using the search word "myopia AND
    prevention" will yield hundreds of studies with similar results. In
    science, when many researchers, repeating similar experiments find similar
    results, the results are believable. Here is my nutshell summary:

    First some terms:
    Hyperopia is defined as an eye too short for its power and images from
    objects at optical infinity are focused behind the retinal plane. Eyes with
    hyperopia have hyperopic blur at all viewing distances.

    Myopia is defined as an eye too long for its power and images from objects
    at optical infinity are focused in front of the retinal plane. Eyes with
    myopia have myopic blur at some viewing distances, have no blur at some
    viewing distances and have hyperopic blur at some viewing distances.

    Emmetropia is defined as an eye the right length for its power and images
    from objects at optical infinity are focused at the retinal plane. Eyes
    with emmetropia have have no blur at some viewing distances and have
    hyperopic blur at some viewing distances.

    Accommodation is the ability of the eye to increase its focal power when
    viewing near objects. This is needed to see clearly at near for emmetropic
    eyes, at far and near for hyperopic eyes and at some near distances for
    myopic eyes.

    Then what is known from the research:
    Neonatal animals are born hyperopic, eye length increases during infancy and
    childhood stabilizing at the point when emmetropia is achieved. Little eye
    growth happens after that point.

    The eye has a mechanism (emmetropization) to determine when emmetropia is
    achieved and in the absence of a signal that emmetropia is present, will
    continue to grow. The mechanism works at the retinal level, is not
    triggered by accommodation and works even with a severed optic nerve. Each
    eye has its own independent control, though there is some small influence by
    each eye upon its fellow. The mechanism works quickly and emmetropia is
    achieved in early childhood.

    The mechanism works by detecting hyperopic or myopic blur and speeding up or
    slowing down the normal rate of growth of the eye. The mechanism can
    detect the difference between hyperopic blur due to hyperopia and hyperopic
    blur due to near viewing; if hyperopic blur is absent for as little as 10%
    to 15% of the time, it will respond minimally to the blur.

    It responds slowly to speed growth when hyperopic blur is present and
    responds quickly to slow growth when myopic blur is present. The mechanism
    is very sensitive to myopic blur; if myopic blur is present for as little as
    10% to 15% of the time, even if hyperopic blur is present for the rest of
    the time, it will respond to the myopic blur and slow growth. The result
    of all this control is that most animals will be emmetropic or slightly
    hyperopic at adulthood.

    The mechanism varies in its speed and precision both within and between
    species. It works well in young animals and less well or minimally in adult
    animals.

    Now my comments. I will play devil's advocate and argue that refractive
    error is genetic and cannot be altered by environment and that this position
    does not violate what is known from the research. I welcome someone else
    taking the other side and arguing that refractive error is environmental and
    can be altered, without violating what is known.

    High hyperopia and high myopia run in families, can be predicted on the
    basis of family history, are associated with various chromosomal
    abnormalities, are more prevelent in premature births or at risk births and
    there is some early work that has identified potential genes.

    Refractive error in adults or non neonates should not exist because
    emmetropization will eliminate it. If refractive error does exist, there
    must be have been a failure of emmetropization. I propose two ways of
    failure.

    First, problems with the rate of growth. The eye may have had an inherited
    abnormal rate of growth (very slow in the case of hyperopia and very fast in
    the case of myopia) beyond the ability of the emmetropization to speed up or
    slow down enough to achieve emmetropization. Or the eye growth mechanism
    has a faulty inherited process and fails to respond to signals from the
    emmetropization mechanism. Or growth continues in late childhood and
    adulthood after the emmetropization mechanism has "turned off" and thus is
    not available for control.

    Second, the eye may have had an inherited ineffective emmetropization
    mechanism, failed to effectively detect blur and thus failed to precisely
    regulate eye growth. There is research evidence that myopic eyes in
    particular are not as sensitive as non myopic eyes in blur detection. Or
    the emmetropization mechanism "turned off" too soon, before adulthood was
    achieved and body growth stopped. Myopia often first appears at puberty,
    when the body is growing rapidly, this myopia may be due to emmetropization
    blur detection ending too soon after sucessful regulation of eye growth in
    babyhood and childhood.

    The existance of refractive error is evidence that emmetropization does not
    work in a particular eye. Environment modification fixes that depend upon
    an intact emmetropization mechanism (such as inducing myopic blur through
    the use of plus lenses) will not work to prevent or reverse refractive error
    in those eyes.

    Dr Judy
     
    Dr Judy, Aug 14, 2004
    #8
  9. Dr Judy

    Cathy Hopson Guest

    That was an excellent presentation. After spending some time fine-tuning my
    point-by-point argument against your stand for genetics only, I realized
    your position is that retinal blur has nothing to do with eye shape or size.
    Generally speaking, genetically preprogrammed shape changes, the eye
    included, begin at puberty and continue at preprogrammed times throughout
    our lives. The discussion of emmetropization failure simply fits into this
    scheme.

    I do believe this violates what is known from the research, even as it's
    summarized in your post above. Those with fully functioning emmetropization
    mechanisms do become myopic. They become myopic and remain myopic if the
    myopia inducing stimulus is not removed for at least 10% to 15% of the time
    they are myopically induced. Is this not environmental? The visual
    environment is overruling the fully functioning genetic emmetropization
    mechanism. The "as much as" factor is not summarized here, but, if it can
    be extrapolated from the plus lens studies, it is slightly over 100%, so
    hardly doable even for some with fully functioning emmetropization
    mechanisms. We know the mechanism is fully functional because emmetropia is
    regained with total removal of the myopia inducement.

    The existence of refractive error is now not evidence that emmetropization
    does not work in a particular eye from a genetic cause any more than it is
    evidence that the required uninduced environment periods have not been
    completed. Human myopes do not remove their myopia inducements, near work
    and lenses, for anywhere near the amount of time indicated might be required
    by the animal studies. From the research, very high plus lenses only serve
    to greatly reduce the amount of time required to jump start an intact
    emmetropization mechanism. No claims are made for a faulty mechanism, but
    without the mere existence of refractive error as evidence of
    emmetropization not working in a particular eye, how do you know the
    difference between genetically faulty and environmentally suppressed?

    Cathy
     
    Cathy Hopson, Aug 16, 2004
    #9
  10. Dr Judy

    Cathy Hopson Guest

    A minus lens is an inducement to maintain myopia, even when the myope did
    not wear glasses to become myopic, because the focal length with full
    correction is infinity, giving the retina a reason to not slow eye growth.
    Of course, this is based on the retina being a believer that it has a
    functioning emmetropization mechanism. With a hyperopization mechanism,
    maybe it would return to unaided emmetropia.

    Cathy
     
    Cathy Hopson, Aug 16, 2004
    #10
  11. emmetropization not working in a particular eye, how do you know the
    They simply do not know, pretending that they know.

    When one speaks too difficult, it is always because he does not know.
     
    Rishi Giovanni Gatti, Aug 16, 2004
    #11
  12. Dr Judy

    Cathy Hopson Guest

    They know. They just can't do anything about it without a clinically useful
    paradigm. Remember, she was playing devil's advocate.

    Cathy
     
    Cathy Hopson, Aug 17, 2004
    #12
  13. It's difficult to follow you because their own clinically useful
    paradigm is wrong: people gets no cure with glasses. This is so plain
    a fact that to mask it they invent plentyful of fallacious theories,
    they talk difficult, and the gullible is cheated.

    In the meantime, eyes deteriorate day by day.

    Imperfect sight is rampant, as is the quality of happiness in the
    average man. Just look at recent statistics, where physicians start
    to put the blame on the "ambient" of living.

    In fact, these great minds cannot see that the source of the misery is
    in eyeglasses and mistreated imperfect sight.

    I don't remember the reference of the last study about happiness but I
    think it will be quickly find on google if you look at it.
     
    Rishi Giovanni Gatti, Aug 18, 2004
    #13
  14. Dr Judy

    Cathy Hopson Guest

    I meant they can't change their methods without the researchers telling them
    to. That's the rule they go by.

    Cathy
     
    Cathy Hopson, Aug 18, 2004
    #14
  15. Dr Judy

    Dr Judy Guest

    major snip
    Do you have any human evidence for this statement? How do we know that the
    emmetropization mechanisms are functioning? Finally, how common is it for
    anyone to not spend at least two to three hours a day at non near tasks.

    Is this not environmental? The visual
    If only myopes have emmetropization mechanisms that can be overruled (since
    emmetropes and hyperopes don't get myopic), then I would argue that the
    myopes have a genetic pre disposition to myopia.

    The "as much as" factor is not summarized here, but, if it can
    If their mechanism is functional, how did they get myopic in the first
    place? At some point they become myopic and they don't get glasses right
    away. So they have myopic blur for distances beyond the far point which
    should stimulate emmetropizaton and eliminate the myopia.

    In office, myopes usually first present at around the -1.00 level, so that
    they have myopic blur for all activities beyond 1 metre. Surely you can't
    believe that they spend 90% of their days looking at things closer than 1
    metre.
    Again, I would argue that most emerging myopes do not read for 90% of waking
    hours.

    From the research, very high plus lenses only serve
    Ahh, the great question! How do you prove the environmental cause? I will
    continue to be the 100% genetic devil's advocate until some one provides
    some convincing environmental evidence.

    Dr Judy
     
    Dr Judy, Aug 18, 2004
    #15
  16. Dr Judy

    Dr Judy Guest

    A corrected myope may have an inducement to maintain myopia, but not an
    inducement to become more myopic. Yet most myopes have a history of
    becoming myopic at puberty, getting correction, then becoming more myopic
    with correction for a few years, then after age 18, ceasing to become more
    myopic. What happens at age 18 that myopia increase ceases?

    Dr Judy
     
    Dr Judy, Aug 18, 2004
    #16
  17. Dr Judy

    Otis Brown Guest

    Dear Judy,

    It does not take a "rocket scientist" to figure this out.

    The ones who go to "work", and stop school, stop
    slow down in there progression.

    The ones who go to West Point or the Naval
    Academy continue downward at a rate
    of -1/3 diopter per year.

    THEIR progression does not stop.

    How you make up your statistics!

    Best,

    Otis
    Engineer
     
    Otis Brown, Aug 19, 2004
    #17
  18. Dr Judy

    Cathy Hopson Guest


    - No human research, as you know. I followed your lead as to which research
    counts.
    - Removal of inducement in the research allowed a return to emmetropia, as
    stated in my previous post.
    - Finally, is 30% common enough? Also, "at least two to three hours a day"
    doesn't mean it's enough for all, as stated in my previous post.


    You're not following the discussion from the research. Emmetropes, not
    myopes, were overruled. No predisposition to myopia is indicated when
    emmetropia is restored after removal of myopia inducements, as stated in my
    previous post.


    90% is a reflection of the "as little as" amount of time required to stall
    progression. Some of the myopically induced emmetropes in the research
    required 7.5 times more time than those who succeeded with the least
    required. This is from the plus lens research that showed a range of 8 to
    60 minutes per day was required to counter rest-of-the-day inducement. Your
    minimum 10% to 15%, a rate of 6 to 9 minutes per hour, is what was required
    using no lenses.


    Not only reading, obviously, and for many, it can't be for more than 50% of
    waking hours if the animal studies are indicative. Certainly the 30% that
    are myopes need closer to 50% of their time spent viewing real distance, not
    just barely over one meter, to keep from progressing due to near work. It's
    likely you would find emmetropes and hyperopes can handle near work at other
    points of the 50% to 90% range, but that's another discussion topic.

    Yes, convincing is difficult even in the face of evidence. Is there too
    much else at stake? Why take the genetic side when no one provides
    convincing genetic evidence? My assignment was to argue that refractive
    error can be altered environmentally without violating what is known. The
    genetic argument in your initial summary is full of "shoulds" and "may
    haves" and contends that a "turned off" mechanism continues to run rampant.
    I hoped you'd give genetic evidence that would exclude environment, not
    parallel it. Oh, well.

    Cathy
     
    Cathy Hopson, Aug 19, 2004
    #18
  19. Dr Judy

    Cathy Hopson Guest

    Thanks for the acknowledgment regarding lenses maintaining myopia. At 18,
    most change environment. This proves a genetic cause, I suppose. Oh, well.

    Cathy
     
    Cathy Hopson, Aug 19, 2004
    #19
  20. Dr Judy

    Dr Judy Guest

    Can you provide any research to back up this assertion. And, of course,
    their is no line of work that involves near point tasks
    Except that in the study you get that stat from, only about 40% of the naval
    cadets got more myopic, the rest didn't. I guess 60% of cadets graduate
    without reading any books.
     
    Dr Judy, Aug 19, 2004
    #20
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